Warzecha Z, Dembiński A, Ceranowicz P, Dembiński M, Cieszkowski J, Konturek S J, Polus A, Pawlik W W, Kuwahara A, Kato I, Konturek P C
Department of Physiology, Jagiellonian University Medical College, Krakow, Poland.
J Physiol Pharmacol. 2006 Sep;57(3):425-37.
Ghrelin, a nature ligand for the growth hormone secretagogue receptor (GHS-R), stimulates a release of growth hormone, prolactin and adrenocorticotropic hormone. Also, ghrelin increases food intake in adult rats and humans and exhibits gastroprotective effect against experimental ulcers induced by ethanol or stress. The aim of present study was to examine the influence of ghrelin administration on gastric and duodenal growth and expression of pepsin and enterokinase in young mature rats with intact or removed pituitary.
Two week after sham operation or hypophysectomy, eight week old Wistar male rats were treated with saline (control) or ghrelin (4, 8 or 16 nmol/kg/dose) i.p. twice a day for 4 days. Expression of pepsin in the stomach and enterokinase in the duodenum was evaluated by real-time PCR.
In animals with intact pituitary, treatment with ghrelin increased food intake, body weight gain and serum level of growth hormone and insulin-like growth factor-1 (IGF-1). These effects were accompanied with stimulation of gastric and duodenal growth. It was recognized as the significant increase in gastric and duodenal weight and mucosal DNA synthesis. In both organs, ghrelin administered at the dose of 8 nmol/kg caused maximal growth-promoting effect. In contrast to these growth-promoting effects, administration of ghrelin reduced expression of mRNA for pepsin in the stomach and was without effect on expression of mRNA for enterokinase in the duodenum. Hypophysectomy alone lowered serum concentration of growth hormone under the detection limit and reduced serum level of IGF-1 by 90%. These effects were associated with reduction in daily food intake, body weight gain and gastroduodenal growth. In hypophysectomized rats, administration of ghrelin was without significant effect on food intake, body weight gain or growth of gastroduodenal mucosa. Also, serum concentration of growth hormone or IGF-1 was not affected by ghrelin administration in rats with removed pituitary.
Administration of ghrelin stimulates gastric and duodenal growth in young mature rats with intact pituitary, but inhibits expression of mRNA for pepsin in the stomach. Growth hormone and insulin-like growth factor-1 play an essential role in growth-promoting effects of ghrelin in the stomach and duodenum.
胃饥饿素是生长激素促分泌素受体（GHS-R）的天然配体，可刺激生长激素、催乳素和促肾上腺皮质激素的释放。此外，胃饥饿素可增加成年大鼠和人类的食物摄入量，并对乙醇或应激诱导的实验性溃疡具有胃保护作用。本研究的目的是探讨胃饥饿素给药对垂体完整或切除的年轻成年大鼠胃和十二指肠生长以及胃蛋白酶和肠激酶表达的影响。
在假手术或垂体切除术后两周，对8周龄的雄性Wistar大鼠腹腔注射生理盐水（对照）或胃饥饿素（4、8或16 nmol/kg/剂量），每天两次，共4天。通过实时PCR评估胃中胃蛋白酶和十二指肠中肠激酶的表达。
在垂体完整的动物中，胃饥饿素治疗增加了食物摄入量、体重增加以及生长激素和胰岛素样生长因子-1（IGF-1）的血清水平。这些作用伴随着胃和十二指肠生长的刺激。表现为胃和十二指肠重量以及黏膜DNA合成的显著增加。在两个器官中，8 nmol/kg剂量的胃饥饿素产生了最大的促生长作用。与这些促生长作用相反，胃饥饿素给药降低了胃中胃蛋白酶mRNA 的表达，并且对十二指肠中肠激酶mRNA的表达没有影响。单独垂体切除将生长激素的血清浓度降低到检测限以下，并使IGF-1的血清水平降低了90%。这些作用与每日食物摄入量、体重增加和胃十二指肠生长的减少有关。在垂体切除的大鼠中，胃饥饿素给药对食物摄入量、体重增加或胃十二指肠黏膜生长没有显著影响。此外，垂体切除的大鼠中胃饥饿素给药对生长激素或IGF-1的血清浓度没有影响。
胃饥饿素给药可刺激垂体完整的年轻成年大鼠胃和十二指肠生长，但抑制胃中胃蛋白酶mRNA的表达。生长激素和胰岛素样生长因子-1在胃饥饿素对胃和十二指肠的促生长作用中起重要作用。
